Lecture 3: Disorders of Tooth Eruption and Shedding PDF

Disorders of eruption and shedding of teeth Predeciduous dentition:  Infants occasionally are born with structures which appear to be teeth Types :  Natal teeth : eruption deciduous teeth present at the time of birth.  Neonatal teeth : deciduous teeth which erupt within first 30 days of l...

Disorders of eruption and shedding of teeth Predeciduous dentition:  Infants occasionally are born with structures which appear to be teeth Types :  Natal teeth : eruption deciduous teeth present at the time of birth.  Neonatal teeth : deciduous teeth which erupt within first 30 days of life. Postpermanent dentition :  It is condition in which several teeth erupt into oral The mandibular incisors, usually one or both central incisors, are cavity after all permanent teeth are lost particularly involved after the insertion of full denture  Premature eruption, natal, and neonatal teeth  Coronal enamel and dentine formation is normal for the chronological age of the tooth, but because of the premature eruption the enamel may be hypoplastic. However, there is usually a virtual absence of root formation and any radicular dentine or cementum that forms is generally irregular in structure due to the mobility of the tooth in the jaw. Premature eruption, natal, and neonatal teeth Premature eruption of other deciduous or permanent teeth is rare and may be related to local factors such as a superficial location of a tooth germ or early shedding of deciduous teeth. Generalized early eruption of the permanent dentition may also be seen in children with endocrine abnormalities associated with an excess secretion of growth hormone or with hyperthyroidism.  Retarded eruption  Endocrinopathies (for example hypothyroidism), prematurity, nutritional deficiencies and chromosome abnormalities, such as Down syndrome, may very occasionally be associated with retarded eruption of either the deciduous and/or permanent dentition. Idiopathic migration, traumatic displacement of tooth germs, or abnormally large crowns may also be associated with retarded-eruption. Delayed eruption and multiple, impacted supernumerary teeth are also a feature of cleidocranial dysplasia  Premature loss: This is usually the result of either dental caries and its sequelae, or chronic periodontal disease. Occasionally, premature loss of teeth is more specifically associated with diseases such as hypophosphatasia, hereditary palmar-plantar hyperkeratosis, and other causes of periodontitis in systemic disease  Persistence of deciduous teeth: This occurs when deciduous teeth are not shed at the expected rime, and is usually associated with the failure of eruption of the permanent successor because it is missing or displaced. Persistence of the entire deciduous dentition is uncommon and usually has a systemic background, such as Cleidocranial dysplasia when eruption of permanent teeth is impeded. Impacted teeth: Teeth which are prevented from eruption into oral cavity by some physical barrier in eruptive path or non availability of space. Causes :  Micrognathia  Retained deciduous teeth  Supernumerary teeth  Odontogenic cyst & tumors  Cleft palate Completely impacted tooth: impacted tooth is totally surrounded by bone. Partially impacted tooth: impacted tooth is partly surrounded by bone & partly by soft tissue Most often affects the mandibular 3rd molars +maxillary canines less commonly: premolars mandibular canines second molars Submerged teeth:  It refers to ankylosed deciduous teeth  Frequently involved teeth are deciduous molars  Occlusal table of the ankylosed deciduous tooth is located below the occlusal plane of the rest of the permanent teeth in the arch giving an submerged appearance  In such cases the underlying permanent tooth may become impacted or may erupt either buccally \ lingually.  Discoloration of Teeth Extrinsic “surface accumulation of Intrinsic “endogenous factors exogenous pigment “ discolorating underlying dentin” 1. Bacterial stains 1. Amelogenesis imperfecta 2. Iron 2. Dentinogenesis imperfecta 3. Tobacco 3. Dental fluorosis 4. Foods and beverages 4. Erythropoietic porphyria 5. Gingival hemorrhage 5. Hyperbilirubinemia 6. Restorative materials 6. Trauma 7. Medications 7. localized red blood cell breakdown 8. Medications Extrinsic staining Chromogenic bacteria  Vary from green or black- brown to orange.  Discoloration occurs most frequently in children  Usually seen initially on the labial surface of max. ant. teeth in gingival 1/3. Plaque-related stains  Black- brown stains.  Most likely are not primarily of bacterial origin but due to formation of ferric sulfide from interaction between bacterial hydrogen sulfide and iron in saliva or gingival crevicular fluid. Tobacco, tea or coffee- related stains  Brown discoloration.  Tar within the tobacco dissolves in saliva and easily penetrates pits and fissures of enamel Amalgam staining  Dental restorative materials especially amalgam, can result in black-gray discolorations of teeth.  This most frequently arises in younger patients who have more open dentinal tubules. Medications  In the past, use of products containing high amounts of iron or iodine was associated with significant black pigmentation of teeth.  More recently, the most frequently reported culprits include stannous fluoride and chlorhexidine. Stannous fluoride  labial surfaces of anterior teeth &occlusal surfaces of posterior teeth. Chlorhexidine  It is associated with yellowish-brown stain at interproximal surfaces near gingival margins Intrinsic staining Congenital porphyria (Gunther disease)  Autosomal recessive disorder of porphyrin metabolism that results in increased synthesis and excretion of porphyrins and their related precursors.  Significant diffuse discoloration of the dentition is noted as a result of deposition of porphyrin in the teeth.  Affected teeth demonstrate a marked reddish- brown coloration that exhibits a red fluorescence when exposed to UV light.  Deciduous dentition is more affected (Enamel &Dentin ). Congenital Hyperbilirubinaemia (Neonatal Jaundice)  Mild transient jaundice is common in neonates but in severe cases, most frequently associated with haemolytic disease of the newborn (rhesus incompatibility), bile pigments may be deposited in the calcifying enamel and dentine of developing teeth, particularly along the neonatal incremental line. The pigment is largely confined to the dentine, the affected teeth being discoloured green to yellowish-brown. . Pulp necrosis is a common cause of a discolored tooth.  Lysis of necrotic tissue and of red blood cells from areas of hemorrhage leads to pigmented products which diffuse into the dentine Congenital Hyperbilirubinaemia (Neonatal Jaundice) Tetracycline staining  Tetracycline intake during pregnancy or childhood- yellowish-grey bands changing into brown.  Permanent incorporation of the antibiotic within the mineral component of calcified tissues.  In UV light showing a bright yellow fluorescence.  Age changes Enamel becomes:  More brittle.  Less permeable. Darker. Dentin:  Continued formation of 2ry dentin with reduction or obliteration of pulp chamber.  Continued formation of peri-tubular dentin results in translucent dentin. Roots become brittle. Cementum:  Continued formation & increased root thickness.  Hypercementosis in presence of other causes. Pulp  Gradual decrease in volume due to 2ry dentin formation.  Decreased vascularity & cellularity.  Increased collagen fiber content.  Impaired response to injury & healing potential.  Increase of pulp stones and diffuse calcification.  Age changes in dentine. The tooth on the left is from an elderly patient and shows attrition, partial obliteration of the pulp chamber, and prominent sclerosis with increased translucency of radicular dentine compared with the younger tooth on the right.  Loss of Tooth Structure Attrition It is the wearing away of teeth because of tooth to-tooth contact Types  Physiological attrition: Attrition which occurs due to normal aging process, due to mastication  Normal occlusal attrition has been calculated at 30 μm/year for molar teeth  Pathological attrition: It occurs due to certain abnormalities in occlusion, chewing pattern or due to some structural defects in teeth.  Etiological Factors for Pathological Attrition 1- Abnormal occlusions  Development: Malocclusion and crowning of teeth, may lead to traumatic contact during chewing, which may lead to more tooth wear  Acquired: Due to extraction of teeth. Extraction causes increased occlusal load on the remaining teeth, as the chewing force for the individual remains constant  Premature contact: In case of edge-to-edge contact, pathological attrition can also occur 2- Abnormal chewing habits: Parafunctional chewing habit like bruxism and chronic persistent chewing of coarse and abrasive food or other substances like tobacco 3- Structural defect: In defects like amelogenesis imperfecta and dentinogenesis imperfecta, hardness of enamel and dentin is reduced and such teeth become more prone to attrition. Clinical features Men usually exhibit more severe attrition than women It may be seen in deciduous as well as permanent dentition. It occurs only on occlusal, incisal and proximal surfaces of teeth Radiographic Features Pulp: Sclerosis of pulp chamber and canals is seen due to deposition of secondary dentin which narrows the pulp canals Periodontal ligament: Widening of periodontal ligament space and hypercementosis Abrasion It is the pathological wearing away of tooth substance through abnormal mechanical process caused by external agents Etiology: Abrasive dentifrices Habitual Occupational Dental floss or tooth picks injury Clinical Features Sites: It usually occurs on exposed surfaces of roots of teeth. It is more commonly seen on left side of right handed persons and vice versa Appearance: In horizontal brushing there is usually a ‘V’ shaped or ‘wedge’ shaped ditch on the root at cementoenamel junction.  The maxillary teeth are more involved than the mandibular Erosion It is the loss of tooth substance by chemical process that does not involve known bacterial action Types (Depending Upon Etiology): Intrinsic: Erosion that occur due to intrinsic causes, e.g. Gastroesophageal reflux, vomiting Extrinsic: Erosion occurring from extrinsic sources, e.g. Acidic beverages, citrus fruits Clinical Features: Sites: It occurs most frequently on labial and buccal surfaces of teeth Appearance: It is usually a smooth lesion which exhibits no chalkiness ,Loss of tooth substance is manifested by shallow, broad, smooth, highly polished and scooped out depression on enamel surface adjacent to cementoenamel junction. Abfraction It is also called as ‘stress lesion’. It is the loss of tooth structure that results from flexure which is caused by occlusal stresses Causes and Mechanism Eccentric forces Occlusal restorations Clinical Features Location: It usually affects buccal/labial cervical areas of teeth. Commonly affects single teeth with excursive interferences or eccentric occlusal loads  The process may affect a single tooth with adjacent teeth being unaffected Resorption of Teeth Physiologic resorption:  Resorption of roots of deciduous teeth prior to shedding.  Transient microscopic areas of superficial resorption of roots of permanent teeth are seen and repaired by cementum or bone-like tissue apposition. Pathologic resorption:  It may start from root surface (external). (More common)  Or it may start from pulpal surface (internal). (Less common)  Osteoclast-like giant cells- odontoclasts are found on dentine surface of the pulp  External resorption: 1. Cysts 2. Dental trauma 3. Excessive mechanical forces (e.g. orthodontic therapy) 4. Excessive occlusal forces 5. Grafting of alveolar clefts 6. Hormonal imbalances 7. Periodontal treatment 8. Peri-radicular inflammation 9. Pressure from impacted teeth 10. Reimplantation of teeth 11. Tumors Radiograph showing external root resorption associated with a periapical granuloma Several forms of external resorption:  Idiopathic lesions (in the cervical areas)  Traumatic incidents (midroot area)  Inflammatory or neoplastic lesions (usually at the apex)  Impacted teeth (mottled radiolucent areas in the crown)  Aggressive orthodontic movement (may exhibit generalized pattern) Extensive burrowing Extensive resorption Extensive resorption of a idiopathic resorption resulting in loss of replanted maxillary involving the cervical region most of the root of a permanent of a central incisor, resulting transplanted maxillary central incisor. in root fracture. canine  Internal resorption: Mostly affects crowns of anterior incisors, Etiology:  Secondary to pulpitis.  Idiopathic (most cases). Clinical features:  Usually asymptomatic, with lesion first detected by appearance of a pink spot (pink tooth of mummery) as the vascular resorptive process approaches the surface).  The resorption continues as long as vital pulp remains.  By this time, extensive loss of tooth structure predisposition to fracture. Radiographic appearance: Fusiform enlargement of pulp chamber in either crown or root. Microscopic appearance:  Loose CT with increased vascularity and few inflammatory cells.  Cases associated with pulpitis, more pulpal inflammation “granulation tissue”.  Odontoclasts-giant cells